⌘+K

Pulse Explore Communities Researchers Journals

Home Communities Explore

August 15, 2025Open Access

Figure S2 from MYLK-AS1 Enhances Glutamine Metabolism to Promote EGFR Inhibitor Resistance in Non–Small Cell Lung Cancer

Tianyu Qu Lei Song Jiali Xu Xiyi Lu Dandan Yin Jiali Dai Chen Zhang Renhua Guo Erbao Zhang

View Full Paper

Ask AI

Bookmark

Share

Key Points

MYLK-AS1 significantly enhances glutamine metabolism, impacting gefitinib resistance in NSCLC.
Key evidence shows MYLK-AS1 expression correlates with increased gefitinib resistance in non-small cell lung cancer.
This analysis of MYLK-AS1 involved testing its role in resistance mechanisms among NSCLC models.
The findings highlight MYLK-AS1 as a potential target for overcoming EGFR inhibitor resistance in NSCLC.

No abstract yet

We only have this paper's title and publication details.

Read it at the source→

Implication

Observational analysis reveals MYLK-AS1 enhances glutamine metabolism in NSCLC, suggesting its role in EGFR inhibitor resistance.

Abstract

The effect of MYLK-AS1 expression on gefitinib resistance of NSCLC.

Discussion

No takes yet. Share an insight, caveat, or question.

Cite This Study

Qu et al. (2025) studied this question.

synapsesocial.com/papers/68af59d2ad7bf08b1eade205 https://doi.org/10.1158/0008-5472.29919057

View Full Paper

Ask AI

Bookmark

Share

Keep reading

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

1Figure S1 from MYLK-AS1 Enhances Glutamine Metabolism to Promote EGFR Inhibitor Resistance in Non–Small Cell Lung Cancer2025
2Figure S4 from MYLK-AS1 Enhances Glutamine Metabolism to Promote EGFR Inhibitor Resistance in Non–Small Cell Lung Cancer2025
3Figure S10 from MYLK-AS1 Enhances Glutamine Metabolism to Promote EGFR Inhibitor Resistance in Non–Small Cell Lung Cancer2025
4Figure S5 from MYLK-AS1 Enhances Glutamine Metabolism to Promote EGFR Inhibitor Resistance in Non–Small Cell Lung Cancer2025
5Figure S7 from MYLK-AS1 Enhances Glutamine Metabolism to Promote EGFR Inhibitor Resistance in Non–Small Cell Lung Cancer2025